Inflammation, Self-Regulation, and Health: An Immunologic Model of Self-Regulatory Failure.

Self-regulation is a fundamental human process that refers to multiple complex methods by which individuals pursue goals in the face of distractions. Whereas superior self-regulation predicts better academic achievement, relationship quality, financial and career success, and lifespan health, poor self-regulation increases a person's risk for negative outcomes in each of these domains and can ultimately presage early mortality. Given its centrality to understanding the human condition, a large body of research has examined cognitive, emotional, and behavioral aspects of self-regulation. In contrast, relatively little attention has been paid to specific biologic processes that may underlie self-regulation. We address this latter issue in the present review by examining the growing body of research showing that components of the immune system involved in inflammation can alter neural, cognitive, and motivational processes that lead to impaired self-regulation and poor health. Based on these findings, we propose an integrated, multilevel model that describes how inflammation may cause widespread biobehavioral alterations that promote self-regulatory failure. This immunologic model of self-regulatory failure has implications for understanding how biological and behavioral factors interact to influence self-regulation. The model also suggests new ways of reducing disease risk and enhancing human potential by targeting inflammatory processes that affect self-regulation.

Better executive function under stress mitigates the effects of recent life stress exposure on health in young adults.

Executive function is a neuropsychological construct that enables controlled cognitive processing, which has been hypothesized to enhance individuals' resilience to stress. However, little empirical work has directly examined how executive function under different conditions mitigates the negative effects of stress exposure on health. To address this issue, we recruited 110 healthy young adults and assessed their recent life stress exposure, executive function in either a stressful or non-stressful context, and current health complaints. Based on existing research, we hypothesized that individuals exhibiting better executive function following a laboratory-based stressor (but not a control task) would demonstrate weaker associations between recent stress exposure and health because they perceived recent life stressors as being less severe. Consistent with this hypothesis, better executive function during acute stress, but not in the absence of stress, was associated with an attenuated link between participants' recent life stress exposure and their current health complaints. Moreover, this attenuating effect was mediated by lesser perceptions of stressor severity. Based on these data, we conclude that better executive function under stress is associated with fewer health complaints and that these effects may occur by reducing individuals' perceptions of stressor severity. The data thus suggest the possibility of reducing stress-related health problems by enhancing executive function.

The effect of negative affect on cognition: Anxiety, not anger, impairs executive function.

It is often assumed that negative affect impairs the executive functions that underlie our ability to control and focus our thoughts. However, support for this claim has been mixed. Recent work has suggested that different negative affective states like anxiety and anger may reflect physiologically separable states with distinct effects on cognition. However, the effects of these 2 affective states on executive function have never been assessed. As such, we induced anxiety or anger in participants and examined the effects on executive function. We found that anger did not impair executive function relative to a neutral mood, whereas anxiety did. In addition, self-reports of induced anxiety, but not anger, predicted impairments in executive function. These results support functional models of affect and cognition, and highlight the need to consider differences between anxiety and anger when investigating the influence of negative affect on fundamental cognitive processes such as memory and executive function. (PsycINFO Database Record

Avoidance-related EEG asymmetry predicts circulating interleukin-6.

Recent research has linked avoidance-oriented motivational states to elevated pro-inflammatory cytokine levels. According to one of many theories regarding the association between avoidance and cytokine levels, because the evolutionarily basic avoidance system may be activated when an organism is threatened or overwhelmed, an associated inflammatory response may be adaptive for dealing with potential injury in such threatening situations. To examine this hypothesis, we tested whether the neural correlate of avoidance motivation associates with baseline levels of the circulating pro-inflammatory cytokine interleukin-6 (IL-6). Controlling for covariates, greater resting neural activity in the right frontal cortex relative to the left frontal cortex-the neural correlate of avoidance motivation-was associated with baseline IL-6. These results thus support the hypothesis that the avoidance motivational system may be closely linked to systemic inflammatory activity.

Anxiety, not anger, induces inflammatory activity: An avoidance/approach model of immune system activation.

Psychological stressors reliably trigger systemic inflammatory activity as indexed by levels of proinflammatory cytokines. This experiment demonstrates that one's specific emotional reaction to a stressor may be a significant determinant of whether an inflammatory reaction occurs in response to that stressor. Based on extant correlational evidence and theory, a causal approach was used to determine whether an avoidant emotion (anxiety) triggers more inflammatory activity than an approach emotion (anger). In an experimental design (N = 40), a 3-way Emotion Condition × Time × Analyte interaction revealed that a writing-based anxiety induction, but not a writing-based anger induction, increased mean levels of interferon-γ (IFN- γ) and interleukin-1ß (IL-1ß), but not interleukin-6 (IL-6) in oral mucous, F(2, 54) = 4.64, p = .01, ηp(²) = .15. Further, self-reported state anxiety predicted elevated levels of proinflammatory cytokines, all ΔR(²) >.06, ps <.04, but self-reported state anger did not. These results constitute the first evidence to our knowledge that specific negative emotions can differentially cause inflammatory activity and support a theoretical model explaining these effects based on the avoidance or approach motivations associated with emotions.

Does cortisol influence core executive functions? A meta-analysis of acute cortisol administration effects on working memory, inhibition, and set-shifting.

The hormone cortisol is often believed to play a pivotal role in the effects of stress on human cognition. This meta-analysis is an attempt to determine the effects of acute cortisol administration on core executive functions. Drawing on both rodent and stress literatures, we hypothesized that acute cortisol administration would impair working memory and set-shifting but enhance inhibition. Additionally, because cortisol is thought to exert different nongenomic (rapid) and genomic (slow) effects, we further hypothesized that the effects of cortisol would differ as a function of the delay between cortisol administration and cognitive testing. Although the overall analyses were nonsignificant, after separating the rapid, nongenomic effects of cortisol from the slower, genomic effects of cortisol, the rapid effects of cortisol enhanced response inhibition, g+ = 0.113, p=.016, but impaired working memory, g+ = -0.315, p=.008, although these effects reversed over time. Contrary to our hypotheses, there was no effect of cortisol administration on set-shifting. Thus, although we did not find support for the idea that increases in cortisol influence set-shifting, we found that acute increases in cortisol exert differential effects on working memory and inhibition over time.

Oxytocin and vasopressin receptor polymorphisms interact with circulating neuropeptides to predict human emotional reactions to stress.

Oxytocin (OT) and a polymorphism (rs53576) in the oxytocin receptor gene (OXTR) have been independently associated with stress reactivity, whereas oxytocin's sister peptide, arginine vasopressin (AVP) and polymorphisms in the vasopressin receptor gene (AVPR1A) have been independently associated with aggressive behavior. In this study, 68 men and 98 women were genotyped for the OXTR rs53576 polymorphism and the AVPR1A RS1 polymorphism. Baseline and poststressor levels of plasma OT, plasma AVP, positive affect, and anger were assessed. Women, but not men, with high levels of poststressor OT and the GG genotype of rs53576 felt the most positive affect after the stressor. Men, but not women, with high levels of poststressor AVP and the 320 allele of the RS1 polymorphism reported more poststressor anger than noncarriers. These data constitute the first evidence that oxytocin and vasopressin receptor genes interact with levels of OT and AVP to predict sex-specific emotional stress responses.

Motivation to control prejudice predicts categorization of multiracials.

Multiracial individuals often do not easily fit into existing racial categories. Perceivers may adopt a novel racial category to categorize multiracial targets, but their willingness to do so may depend on their motivations. We investigated whether perceivers' levels of internal motivation to control prejudice (IMS) and external motivation to control prejudice (EMS) predicted their likelihood of categorizing Black-White multiracial faces as Multiracial. Across four studies, IMS positively predicted perceivers' categorizations of multiracial faces as Multiracial. The association between IMS and Multiracial categorizations was strongest when faces were most racially ambiguous. Explicit prejudice, implicit prejudice, and interracial contact were ruled out as explanations for the relationship between IMS and Multiracial categorizations. EMS may be negatively associated with the use of the Multiracial category. Therefore, perceivers' motivations to control prejudice have important implications for racial categorization processes.

Neural and behavioral bases of age differences in perceptions of trust.

Older adults are disproportionately vulnerable to fraud, and federal agencies have speculated that excessive trust explains their greater vulnerability. Two studies, one behavioral and one using neuroimaging methodology, identified age differences in trust and their neural underpinnings. Older and younger adults rated faces high in trust cues similarly, but older adults perceived faces with cues to untrustworthiness to be significantly more trustworthy and approachable than younger adults. This age-related pattern was mirrored in neural activation to cues of trustworthiness. Whereas younger adults showed greater anterior insula activation to untrustworthy versus trustworthy faces, older adults showed muted activation of the anterior insula to untrustworthy faces. The insula has been shown to support interoceptive awareness that forms the basis of "gut feelings," which represent expected risk and predict risk-avoidant behavior. Thus, a diminished "gut" response to cues of untrustworthiness may partially underlie older adults' vulnerability to fraud.

Effects of a supportive or an unsupportive audience on biological and psychological responses to stress.

Although social support is related to substantial benefits for health and well-being, research has uncovered qualifications to its benefits. In a test of the psychological and biological impact of an audience on responses to laboratory stress challenges, 183 participants going through the Trier Social Stress Test experienced either (a) an unsupportive audience, (b) a supportive audience, or (c) no audience. Both audience conditions produced significantly stronger cortisol, heart rate, and blood pressure responses to the stress tasks, relative to the no-audience control, even though the supportive audience was rated as supportive. Contrary to hypotheses offered by several theories, these effects were not moderated by self-esteem, individual differences in psychological resources, or baseline social support. Psychological resources and baseline social support were, however, tied to more beneficial biological and psychological profiles at baseline and at recovery in some cases. It was concluded that when one must perform stressful tasks in front of an audience, evaluative concerns may outweigh the potential benefits of a supportive audience.

Anger and fear responses to stress have different biological profiles.

In contrast to a general model of stress, a functional model suggests that emotions may regulate stress responses in specific adaptive ways. The current study examined whether anger and fear during a challenging stress task (Trier Social Stress Task) were differentially associated with cortisol and proinflammatory cytokine responses to an acute stressor. Baseline anger and fear were related to greater cortisol and proinflammatory cytokines. However, anger reactions to the stressor were associated with greater stress-related increases in cortisol over time but not proinflammatory cytokines. In contrast, fear reactions to the stressor were associated with increases in stress-related proinflammatory cytokines over time and a decrease in cortisol. Results are consistent with the functional perspective that distinct emotional experiences appear to trigger temporally-patterned adaptive biological processes to mobilize energy in response to anger and to promote withdrawal in response to fear. Discussion focuses on the role of the HPA axis to increase available metabolic fuel and proinflammatory cytokines to prompt behavioral withdrawal.

The impact of repetition-induced familiarity on agreement with weak and strong arguments.

Repeated statements are perceived as more valid than novel ones, termed the illusion of truth effect, presumably because repetition imbues the statement with familiarity. In 3 studies, the authors examined the conditions under which and the processes by which familiarity signals from repetition and argument quality signals from processing of message content influenced agreement with persuasive arguments. Participants with low or high motivation to process information were presented persuasive arguments seen once or twice. In all 3 studies, repetition increased the persuasiveness of weak and strong arguments when little processing of message content occurred. Two of the studies used a process dissociation procedure to reveal that both greater controlled processing (which reflected argument content) and the greater automatic influence of familiarity (which reflected repetition) were associated with increased acceptance of strong arguments but that greater controlled processing dissipated the benefits of familiarity for agreement with weak arguments.

Thinking straight while seeing red: the influence of anger on information processing.

Because angry people apparently rely on heuristic cues when making judgments, anger has been claimed to trigger superficial, nonanalytic information processing. In three studies, the authors found that induced anger promoted analytic processing. Experiment 1 showed that angry participants were more likely to discriminate between weak and strong arguments than participants in neutral moods. Experiment 2 demonstrated that anger overrode dispositional preferences not to process, causing even those low in need for cognition to process analytically. Experiment 3 reconciled these findings with previous work by showing that angry people used accessible, valid, and relevant heuristics but otherwise processed analytically, as indicated by attitude change and elaboration data. Together, these experiments showed that angry people can have both the capacity and motivation to process and that their selective use of heuristics reflects the cue's perceived validity and not the failure to process analytically.